Jodie M Burton

St. Michael's Hospital, Toronto, Ontario, Canada

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Publications (6)34.31 Total impact

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    ABSTRACT: To characterize the effect of vitamin D(3) intake on urinary calcium:creatinine ratios across predefined ranges of serum 25(OH)D. Patients with multiple sclerosis (n=25) received escalating doses of vitamin D(3) (4000-40,000IU/d) with calcium (1200mg/d). Urinary calcium:creatinine was driven by increased 25(OH)D when concentrations were <75nmol/L (r=0.424, p=0.009) and >200nmol/L (r=0.281, p=0.01), but no relationship existed when 25(OH)D concentrations were 76-200nmol/L. A "safe", physiological range of 25(OH)D concentrations is 75-200nmol/L.
    Clinical biochemistry 07/2011; 44(10-11):930-2. · 2.02 Impact Factor
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    ABSTRACT: The active metabolite of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)(2)D], is a potent modulator of immune cells in vitro. Our objective was to determine whether the sun-dependent nutrient, cholecalciferol, can alter disease-associated cellular immune abnormalities in patients with multiple sclerosis (MS). This was an open-label, 12-month, randomized controlled trial. Patients with MS were recruited from the MS Clinic at St. Michael's Hospital, Toronto. Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group). Treated patients received increasing doses of cholecalciferol (4,000-40,000 IU/d) plus calcium (1200 mg/d), followed by equilibration to a moderate, physiological intake (10,000 IU/d). Control patients did not receive supplements. At enrollment and at 12 months, peripheral blood mononuclear cell (PBMC) proliferative responses to disease-associated, MS-relevant, and control antigens were measured, along with selected serum biochemical markers. At 12 months, mean serum 25-hydroxyvitamin D [25(OH)D] concentrations were 83 ± 35 nmol/liter and 179 ± 76 nmol/liter in control and treated participants, respectively (paired t, P < 0.001). Serum 1,25(OH)(2)D did not differ between baseline and 1 yr. In treated patients, 12-month PBMC proliferative responses to neuron antigens myelin basic protein and exon-2 were suppressed (P = 0.002). In controls, there were no significant changes in disease-associated PBMC responsiveness. There were no significant differences between groups in levels of selected biomarkers. MS-associated, abnormal T cell reactivities were suppressed in vivo by cholecalciferol at serum 25(OH)D concentrations higher than 100 nmol/liter.
    The Journal of Clinical Endocrinology and Metabolism 06/2011; 96(9):2826-34. · 6.31 Impact Factor
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    ABSTRACT: Low vitamin D status has been associated with multiple sclerosis (MS) prevalence and risk, but the therapeutic potential of vitamin D in established MS has not been explored. Our aim was to assess the tolerability of high-dose oral vitamin D and its impact on biochemical, immunologic, and clinical outcomes in patients with MS prospectively. An open-label randomized prospective controlled 52-week trial matched patients with MS for demographic and disease characteristics, with randomization to treatment or control groups. Treatment patients received escalating vitamin D doses up to 40,000 IU/day over 28 weeks to raise serum 25-hydroxyvitamin D [25(OH)D] rapidly and assess tolerability, followed by 10,000 IU/day (12 weeks), and further downtitrated to 0 IU/day. Calcium (1,200 mg/day) was given throughout the trial. Primary endpoints were mean change in serum calcium at each vitamin D dose and a comparison of serum calcium between groups. Secondary endpoints included 25(OH)D and other biochemical measures, immunologic biomarkers, relapse events, and Expanded Disability Status Scale (EDSS) score. Forty-nine patients (25 treatment, 24 control) were enrolled [mean age 40.5 years, EDSS 1.34, and 25(OH)D 78 nmol/L]. All calcium-related measures within and between groups were normal. Despite a mean peak 25(OH)D of 413 nmol/L, no significant adverse events occurred. Although there may have been confounding variables in clinical outcomes, treatment group patients appeared to have fewer relapse events and a persistent reduction in T-cell proliferation compared to controls. High-dose vitamin D (approximately 10,000 IU/day) in multiple sclerosis is safe, with evidence of immunomodulatory effects. This trial provides Class II evidence that high-dose vitamin D use for 52 weeks in patients with multiple sclerosis does not significantly increase serum calcium levels when compared to patients not on high-dose supplementation. The trial, however, lacked statistical precision and the design requirements to adequately assess changes in clinical disease measures (relapses and Expanded Disability Status Scale scores), providing only Class level IV evidence for these outcomes.
    Neurology 06/2010; 74(23):1852-9. · 8.25 Impact Factor
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    ABSTRACT: Multiple Sclerosis (MS), a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS), is characterized by recurrent relapses of CNS inflammation ranging from mild to severely disabling. Relapses have long been treated with steroids to reduce inflammation and hasten recovery. However, the commonly used intravenous methylprednisolone requires repeated infusions with the added costs of homecare or hospitalization, and may interfere with daily responsibilities. Oral steroids have been used in place of intravenous steroids, with lower direct and indirect costs. The primary objective was to compare efficacy of oral versus intravenous steroids for MS relapses <= 6 weeks. Secondary comparisons included subsequent relapse rate, disability, ambulation, hospitalization, immunological markers, radiological markers, and quality of life. A literature search was performed using Cochrane MS Group Trials Register (July 2008), Cochrane Central Register of Controlled Trials (CENTRAL) "The Cochrane Library 2008, issue 3, MEDLINE (PubMed) (1966-July 2008), EMBASE (1980-July 2008), abstracts from meetings of the American Academy of Neurology (2002-2008), the European Federation of Neurological Sciences (2002-2008), the European Committee for Treatment and Research in Multiple Sclerosis and American Committee for Treatment and Research in Multiple Sclerosis (2002-2008) handsearching. No language restrictions were applied. Randomized or quasi-randomized trials comparing oral and intravenous steroids for acute relapses (<=30 days) in clinically definite MS patients over age 16 were eligible. Methodological was assessed using trial publications and personal communication. Elevant data was extracted, and effect size was reported as mean difference (MD),weighted mean difference (WMD), odds ratio (OR) and absolute risk difference (ARD). Eligible studies (167 patients) were identified. Only one outcome, the proportion of patients with EDSS improvement at 4 weeks, was common to three trials. Otherwise outcomes were too heterogeneous to pool. Only one trial employed an equivalence design, but all reported no statistically significant difference in outcomes between groups. Namely, there was no significant difference in the degree of recovery 4 weeks following treatment. No difference was found in subsequent relapse rate, disability, hospitalization, ambulation, bioavailability, or in magnetic resonance imaging (MRI). Due to methodological limitations, heterogeneous treatment regimens and limited data, formal conclusions about equivalence of oral and intravenous steroidscannot be made. Oral Megadose Corticosteroid Therapy of Acute Exacerbations of Multiple Sclerosis (OMEGA) trial, designed to address such limitations, is currently underway. The trials reviewed support the hypothesis that no significant differences in clinical, radiological or pharmacological outcomes oral and intravenous steroids for MS relapses exist. However, with the small number of patients and methodological limitations, conclusions of equivalence are premature.
    Cochrane database of systematic reviews (Online) 01/2009; · 5.70 Impact Factor
  • Neurology 12/2008; 71(22):1833-4. · 8.25 Impact Factor
  • Jodie M Burton, Paul O'Connor
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    ABSTRACT: In 1993, interferon beta-1b, the first clinically proven disease-modifying agent for multiple sclerosis, was approved, with several comparable agents following close behind. These agents have been beneficial in reducing relapse events and MRI lesions, but all require parenteral administration, leading some otherwise eligible patients to decline such therapies. Oral agents have been studied for decades with mixed results, but a small number of medications currently being tested in phase II/III clinical trials have shown promise in efficacy and tolerability. This review assesses the results of the more thoroughly studied of these agents, some of which may soon be approved for use in multiple sclerosis.
    Current Neurology and Neuroscience Reports 06/2007; 7(3):223-30. · 3.78 Impact Factor